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The severe posterior hypothalamic atrophy in the FTLD-TDP group was associated with neuronal loss and sparse pathology (see above).
Examination of the dorsal subiculum (Bregma −2.50) showed strong evidence of propagation in P301SBE mice, whereas control mice showed only sparse pathology (Fig. 3b).
The laminar distribution of pathology was difficult to observe at low magnification due to the presence of nuclei staining in normal neurons, and remained difficult at higher magnifications, particularly in cases with sparse pathology.
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Thus, assessment of oligomeric Aβ in individuals with sparse HPτ pathology should urgently be carried out.
In contrast, sparse basal forebrain pathology (range of 2 3 NCIs in three HPFs) occurred in three cases without hypothalamic pathology.
The suggestion of prion-like propagation of neurodegeneration would be in line with the former interpretation [ 13] whereas the observation of sparse extent of pathology in most aged subjects supports the latter.
Increasing the treatment to 25 μg fibrillar 21 140 αS resulted in sparse brain αS pathology as early as 1 month and 4 months, but it was extensively distributed throughout the neuroaxis by 8 months (Table 2, Figures 4 and 5) at a higher density than in nTg mice showing αS pathology at 8 months post-injection of 25 μg fibrillar 21 140 αS.
However, evidence that these processes are associated with regional postmortem Aβ pathology is sparse.
Bunina bodies were found in all cases with FTLD-MND, except one case who showed very subtle lower motor neuron neuronal loss and sparse TDP-43-positive pathology.
We also screened for intracellular inclusions in other brain regions and could not demonstrate abnormality other than sparse Alzheimer and LB pathology.
This may be due to sparse training in epilepsy pathology and or due to lack of neuropathological guidelines for companion animals.
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